You are on page 1of 6

MSJA RESEARCH PAPERS

An overview of liver trauma


Christian Beardsley* and Sivakumar Gananadha**
*

Medical Student, The Australian National University

**

Staff Specialist, Upper GI/HPB Unit, The Canberra Hospital

he liver is the largest solid organ


within the abdominal cavity,
and combined with the great
surface area of the trunk, explains why
this critical organ is often injured. Liver
injury is a significant cause of morbidity
and mortality in trauma patients, both
in the civilian and military context. The
dynamics of society and technology
are constantly evolving, and so are the
dynamics of liver trauma. Liver surgery
has become safer with lower morbidity
and mortality and this has influenced
the management of liver trauma, which
has changed considerably since the
20th century. This overview is intended
for the everyday doctor, who may in
their practice encounter the seriously
traumatised patient with a liver injury.
SURGICAL MANAGEMENT OF LIVER
TRAUMA IN THE PAST
Research into the surgical management
of liver injuries started to boom in the
early twentieth century, and this was
strengthened and driven by the impact
of the world wars. Pringles famous
manoeuvre was performed in 1908,
and the concept of perihepatic packing
became fashionable during World War
(WW) I (1). After the impact of WW II,
surgeons turned to more aggressive
forms of management for liver trauma.
Hepatic resections, hepatic artery ligation
and mattress suture became mainstay
treatment modalities used by surgeons,
in an attempt to save the rapidly
exsanguinating patient. In 1968, Shrock
and colleagues pioneered the use of the
atriocaval shunt, a complex procedure
developed as a last ditch strategy to try
and salvage a desperate situation (2). It
thus shocked many a trauma surgeon
when non-operative management
(NOPM) was reported as a potentially

ABSTRACT
Even with todays modern surgical techniques and sophisticated intensive
care units, management of the traumatic liver injury still represents a
major challenge to the most highly experienced trauma surgeons. In the
last century, there was constant debate regarding the most appropriate
management of these often critically ill patients. This is because hepatic
injuries carry the potential for catastrophic exsanguination due to the highly
vascular nature of this organ. Mortality and morbidity rise dramatically after
high grade liver injury, but often these result from the associated injuries
incurred due to the mechanism and severity of the injury. In Australia,
blunt trauma is the predominant mechanism of injury, often from high
speed motor vehicle accidents. However, in other parts of the world and
particularly in areas of conflict, penetrating trauma represents a significant
cause of hepatic trauma. This article provides an overview for health care
professionals, who in their every day practice may encounter the patient
with hepatic trauma.
successful treatment modality for
blunt liver trauma (3-5). This treatment
strategy gained momentum in the late
80s and within a decade had become the
mainstay strategy for managing blunt
liver trauma. It is intriguing that as early
as 1887; Edler was reportedly managing
several hundreds of patients with liver
trauma non-operatively (3).
EPIDEMIOLOGY AND
PATHOPHYSIOLOGY
The anatomical location of the liver, its
size and the large surface area of the
upper abdomen and trunk account for
the high proportion of liver injuries seen
in trauma patients suffering from both
blunt and penetrating trauma (6-9). The
spleen and kidneys are the other solid
organs commonly involved under these
circumstances. Moores grading system
for liver trauma, which depicts the range
of injuries which can be sustained to a
patients liver, is presented in Table 1 (10).
Grade

indicates

minor

injury

MSJA Volume 3 Issue 1 June 2011

represented by simple haematoma


whilst Grade V indicates a severe
injury with laceration of the liver and
possible vascular involvement. Grade VI
represents total hepatic avulsion and
is considered to be incompatible with
life. It is worth noting that up to 80% of
liver injuries are of a minor grade and
do not require operative management
(4,9,11,12) . This is in stark contrast
to higher grades (Grade IV and V)
which often require prompt operative
intervention (6,12,13). It is also worth
noting that whilst with splenic trauma,
higher grades are associated with
failure of NOPM, some high grade
hepatic injuries can be managed
conservatively (14).
The incidence of liver trauma varies
between countries due to social,
regulatory
and
environmental
conditions. In Europe, 80-90% of
all hepatic injuries are due to blunt
trauma, with the majority of cases
being due to road traffic accidents,
sporting injuries and falls (6,14).
5

MSJA RESEARCH PAPERS

Table 1: Grading of Liver Trauma (adapted from the American Association for the Surgery of Trauma (AAST) guidelines (10)

Grade

Injury

Description

Haematoma

-Subscapular, less than 10% of surface area


-Capsular tear, less than 1 cm Parenchymal depth

Laceration
II

III

Haematoma

-Subcapsular, 10-50% of surface area.

Laceration

-Intraparenchymal, less than 10 cm in diameter


1-3cm parenchymal depth, less than 10cm in diameter

Haematoma

-Subcapsular, more than 50% Surface area or expanding


-Ruptured subscapsular, or parenchymal haematoma
-Intraparenchymal, more than 10 cm or expanding
More than 3cm parenchymal depth

Laceration

IV

Laceration

-Parenchymal disruption, involving more than 75% of hepatic lobe


-One to three Couinaud segments within a lobe

Laceration
Vascular

-Parenchymal disruption involving more than 75% of hepatic lobe


-More than three Couinaud segments within a single lobe
Juxtahepatic venous injuries, i.e., retrohepatic cava/central major hepatic veins

Vascular

Hepatic avulsion

VI

This situation is similar to that seen in


Australia. In contrast, the United States
and South Africa have relatively high
rates of penetrating trauma (4,6). Yet
even in these countries there is evidence
that the ratio of blunt to penetrating
injury is increasing (4,8). Hepatic injuries
are associated with high mortalities, but
it remains very difficult to prognosticate
for individual patients, because mortality
is often determined by numerous factors
including the nature of the hepatic injury
itself, grade of hepatic injury, associated
injuries
incurred,
practices
and
experiences of the treating institution
and the physiological characteristics of
the patients themselves (8,12-14). Overall
mortality from liver injuries is estimated
to range from 10-17% (6,8). However,
if a patient has sustained juxtahepatic
venous injury (retrohepatic inferior vena
cava or central major hepatic venous
injury) then mortality may be as high as
80% (13).
Blunt liver trauma is a common injury in

civilian life, largely attributable to road


traffic accidents. The liver is snuggled
tightly under the diaphragm and thus a
compressive force directed at the upper
abdomen can result in a crush injury to
the liver due to the uncompromising
nature of the liver capsule (6,13). The
liver can also be injured by deceleration
injuries which tear the liver from its
supporting structures. The spine can also
act as an anvil, leading to a compression
injury due to an antero-posteriorly
directed force.
Penetrating trauma is due to stab
wounds and gunshot wounds, the latter
being relatively uncommon in Australia
due to stringent fire arm legislations.
Stab wounds lead to injury along the
trajectory whilst gunshot wounds lead
to a trajectorial injury and a secondary
injury to the related blast effect (15).
Whilst the liver receives protection from
overlying ribs, a force directed at the
right upper quadrant can compress the
ribs into the liver resulting in a bear clawinjury, generally to the right lobe of the

MSJA Volume 3 Issue 1 June 2011

liver (13).
ASSOCIATED INJURIES
Any injury which is significant enough
to cause liver trauma often causes
multiple injuries to other viscera and
body regions. Over 80% of patients
with liver injuries may have one
or more associated injuries (5). In
blunt hepatic trauma, chest injuries
are the most commonly associated
injury followed by long bone and
pelvis fracture, intrabdominal solid
organs (spleen) and head injuries
(5). In penetrating trauma, the small
bowel, colon, diaphragm, stomach
and kidneys are commonly involved
whilst the spleen and pancreas are
uncommonly injured (5,7). Ultimately
it is these injuries which can lead to a
detrimental or fatal outcome for the
patient. Injury to vascular structures
carries a particularly dire prognosis
(5,7,12). In fact, the presence of a major
abdominal vascular injury (the inferior

MSJA RESEARCH PAPERS

vena cava, aorta, and portomesenteric


vessels) is associated with a 50% increase
in mortality compared to patients
without such injuries (5).
PATIENT ASSESSMENT AND INITIAL
MANAGEMENT
Any patient suffering from trauma
should be managed in accordance with
guidelines set out in the Advanced Trauma
Life Support (ATLS) and Emergency
Management of Severe Trauma (EMST)
programs run respectively by the
American College of Surgeons and the
Royal Australasian College of Surgeons.
Primary survey, with plain chest X- ray
and Focused Abdominal Sonography for
Trauma (FAST) serving as useful adjuncts,
must be conducted with the priority
being determination of a correctable
major injury. Diagnostic peritoneal
lavage has largely been superseded by
FAST, however it remains a useful test
for the rural or remote practitioner (6).
If a FAST scan is positive and the patient
is haemodynamically unstable, then
operative management must not be
delayed by radiological assessment (13).
If the FAST is positive but the patient is
haemodynamically stable, CT scan is the
gold standard investigation to perform
and may assist management by helping
to delineate the extent of the injury
and any associated injuries incurred,
thus further directing management
(6,11). Patients should be adequately
resuscitated but a haemodynamically
unstable patient should not have
their operations delayed.
Indeed,
there is evidence that overaggressive
resuscitation may lead to exacerbation
of haemorrhage, potentially through
the dislodgement of a previously
tamponading clot (6). However, the
development of the shock triad (acidosis,
coagulopathy and hypothermia) must
be avoided as this is strongly correlated
with mortality and hence resuscitation
must be adequate (7,9,15). The massive
transfusion protocol must be activated.
Intra-Venous access must be obtained
above the diaphragm as clamping of the
retrohepatic vena cava may negate any
utility of sub-diaphragmatic routes.

Table 2: Criteria for Non-Operative Management in Liver Trauma

Criteria for non Operative Management:


(1) haemodynamic stability, or stability achieved with minimal resuscitation
(1-2 litres of crystalloid)
(2) absence of other abdominal injuries requiring laparotomy
(3) preserved consciousness allowing serial examination of abdomen
(4) absence of peritonism
(5) absence of ongoing bleeding on CT scan
DEFINITIVE MANAGEMENT:
(1) NON-OPERATIVE MANAGEMENT
NOPM of liver trauma has gained
acceptance due to a substantial body of
evidence which has demonstrated the
success of this strategy when applied to
carefully chosen patients (3-6,8,13). Its
use is now widespread and indeed up to
80% of patients with hepatic injuries can
now be managed conservatively (4,5).
However, this treatment strategy does
have complications, and the failure rate
varies from seven to twelve percent (5,8).
Criteria for NOPM are found in Table 2.
Interventional
techniques
such
as angiography and embolization
and
Endoscopic
Retrograde
Cholangiopancreatography (ERCP) with
stent placement also play a major role in

the NOPM of liver injuries. Angiographic


embolisation may be useful when
there is evidence of contrast blush
on the CT and/or evidence of
haemobilia (presenting clinically
with jaundice, and gastrointestinal
bleeding), whilst ERCP with stenting
is useful for bile leaks (see Figures 1,
2). Such techniques are of use in the
haemodynamically stable patient, or
in the patient who has been managed
by packing techniques, and may
help avoid the morbidity associated
with further operative intervention
(3,4,6,11,13). Proponents of NOPM
have advocated that this strategy has
been successful partly due to modern
resuscitation techniques and the livers
regenerative capabilities (2,4,5,9,13).
Because the venous system is low

Figure 1: Transverse CT scan of a patient with severe blunt hepatic trauma showing extensive
haematoma and arterial blush (grade IV). The patient underwent angiography with succesful
embolisation of the bleeding vessel. Source: courtesy of Dr. Sivakumar Gananadha, Upper
Gastrointestinal Unit, The Canberra Hospital

MSJA Volume 3 Issue 1 June 2011

MSJA RESEARCH PAPERS

Figure 2: Coronal CT scan of the same patient in figure 1 demonstrating the arterial blush (arrow).
Source: Courtesy of Dr. Sivakumar Gananadha, Upper Gastrointestinal Unit, The Canberra Hospital

pressure, operative intervention may


worsen the haemodynamic situation by
dislodgement of a previously stabilising
clot on exploration of the wound thus
leading to catastrophic haemorrhage (4).
It is worth noting that this management
style has gained acceptance for the
management of blunt trauma in children
and adults alike but applicability in the
management of penetrating hepatic
trauma remains questionable (3,7).
DEFINITIVE MANAGEMENT:
(2) OPERATIVE MANAGEMENT OF
LIVER TRAUMA
As mentioned previously, operative
management of liver trauma has declined
significantly over the past two decades,
with the realisation that many hepatic
injuries can be treated conservatively
with
medical
management
and
interventional procedures (4). Indications
for operative intervention are found
in Table 3. It is also worth noting that
operative management of liver trauma
has evolved. The utilisation of complex
procedures to gain haemodynamic
stability such as atriocaval shunts
and selective hepatic artery ligation,
have largely been superseded by the
philosophy of damage control surgery
(DCS) (4,13). However, indications for
such procedures still exist but these
techniques are best left to the hepatopancreato-biliary surgeon or after all

other options have been exhausted.


Damage control surgery, as defined
by Rotondo et al., is the initial control
of haemorrhage and contamination
followed by intraperitoneal packing and
rapid closure, allowing for resuscitation
to normal physiology in the intensive
care unit and subsequent definitive
re exploration (16). Practically this
embodies techniques aimed at halting
haemorrhage and correcting any enteric
spills (7). Once the abdomen is packed,
optimal conditions are now present
for anaesthetic resuscitation of the
patient. If haemostasis is controlled,
the patient should be closed and sent
to the ICU. However, if the patient is
still haemodynamically unstable, a
substantial problem awaits the surgeon.
In the case of a general surgeon in a
lower tier Trauma Centre, transfer to a
Level I Trauma Centre with a specialist
liver surgery unit is advisable (9). There
is substantial evidence to indicate that
mortality is reduced when hepatopancreato-biliary surgeons manage
liver trauma, and thus transfer should
be undertaken as soon as the patient is
haemodynamically stable (6,9,13).
It is outside of the scope of this article
to describe the interventions necessary
when initial measures fail, but briefly
techniques such as Pringles manoeuvre
(clamping of the hepatoduodenal

MSJA Volume 3 Issue 1 June 2011

ligament),
simple
suture
and
compression, hepatotomy and vascular
ligation, and finally, in the most dire
of circumstances the atriocaval shunt
may be employed as a last ditch effort
to obtain haemodynamic control.
Stone et al. advised that for the surgeon
faced with the desperate situation in
the operation room, the use of sutures
on a large curved needle combined
with packing is advised (9). Whilst
the choice of technique to achieve
haemostasis after packing still remains
contentious, what is not debated is
that proper resuscitation and warming
of the patient (and crucially, blood
products and fluids) is paramount to
the patients survival (9,13).
COMPLICATIONS
FOLLOWING
MAJOR HEPATIC INJURY
Whilst the major acute risk for these
patients is exsanguination, a large
proportion of deaths are attributable
to associated injuries incurred in the
accident, multi-organ failure, sepsis,
pneumonia and acute respiratory
distress (5,13). Late complications
include hepatic necrosis, bile duct
leakage, and intra-abdominal abscess.
MANAGEMENT
OF
INJURIES IN CHILDREN

HEPATIC

In children, most abdominal injuries


are caused by motor vehicle accidents
followed closely by bicycle and sporting
injuries (17). NOPM of blunt abdominal
injuries was a concept pioneered
by paediatric surgeons (18,19). The
previously mentioned caveats apply,
but by and large its utilisation is well
documented for the management of
children with blunt abdominal trauma.
Two landmark papers established nonoperative intervention as a successful
management strategy for blunt
abdominal trauma in the paediatric
population (20,21). In contrast, the
management of penetrating injuries
in children is still debatable, due to
the anatomical differences between
children and adults. In the adult,
the relative size of the liver, acts as
a buffer and protects other viscera
from injury. However, in children

MSJA RESEARCH PAPERS

due to the increased compactness


of the abdominal compartment, the
likelihood of multi-viscera injury is
particularly high.
Sadly in the United States, firearms
account
for
the
predominant
mechanism of penetrating injury in
children and adolescents, followed
closely by stabbing and impalements
(22,23).
For penetrating injuries,
Dicker et al. found that 43% of patients
required repair of hepatic injuries, and
that an alarming rate of children (49%)
had associated abdominal injuries (19).
The stomach, small and large intestine
followed by the spleen and kidneys
were the most frequently injured
viscera (18). Thus the preponderance
of associated injuries, the effects of
the primary injury, and the compact
anatomical nature of children may
in itself obligate a more aggressive
operative approach in penetrating
trauma to children (18,19,22).
DISCUSSION
Over the past three decades, the
management of liver trauma has
changed dramatically. Yet the overall
burden of liver trauma, as well as
the severity of injuries occurring
has not (4,5,7). The advent of fast,
reliable and high resolution CT
scanners has enabled non-operative
management of blunt liver trauma
to become the mainstay. However,
several caveats must be observed
before non-operative therapy can be
employed. Firstly the patient must
be haemodynamically stable, and
this must not come at the price of
aggressive resuscitation. The need
for blood transfusion may be an early
indication for conversion to operative
management (11,13,24). Secondly,
serial abdominal examinations must
be able to be performed, and if any
signs of peritonism develop, operative
intervention should not be delayed.
Thirdly, there must be the absence
of the following CT findings: contrast
pooling or arterial blush not alleviated
with angiographic techniques (11).
Whilst penetrating trauma is not by
itself an absolute contraindication to

Table 3: Criteria for Operative Management in Liver Trauma

Criteria for Operative Management (4,6,13,14):


(1) any patient who is haemodynamically unstable with suspected liver trauma
(2) multiple transfusions required to maintain haemodynamic stability
(3) signs of peritonism, or development of peritonism on serial abdominal examinations
(4) active arterial blush on CT for which interventional techniques have failed
and/or ongoing bleeding on CT scan with focal pooling of contrast
(5) penetrating trauma
non-operative management, it usually
warrants a more aggressive approach
(2). Whilst more severe AAST liver grade
injuries usually correlate with increased
morbidity and mortality, some of
these patients can be managed with
conservative therapy (4,5).
The importance of detecting associated
injuries is also paramount as these
frequently play an equal role as the liver
injury does with regards to mortality
(12,14).
It is also worth noting that the following
factors are predictors of NOPM failure:
haemodynamic instability; liver injury
AAST of Grade IV or V; and pooling of
contrast on CT scan (14). Adequate,
but not over-aggressive, resuscitation
is also a must to maximise the patient
outcome. Oxygenation, and correction
of
hypovolemia,
hypothermia,
coagulopathy and acidosis are critical in
the care of the hepatic trauma patient
(6,9,13). The concept of damage control
surgery has also helped to improve the
prognosis of the patient with hepatic
trauma. Only interventions which correct
haemorrhage and enteric spill are
carried out during DCS, whilst delaying
definitive surgical management until the
patient is adequately resuscitated. This
is a particularly wise strategy when the
hospital is not a major trauma centre,
and transfer to a specialist liver unit is
necessary. Abdominal and perihepatic
packing have become the main
techniques in the initial management
of exsanguinating liver trauma, with
more elaborate techniques being

MSJA Volume 3 Issue 1 June 2011

best left to liver unit specialists. It is


also worth noting that whilst nonoperative management has become
the dominant treatment modality, the
mortality rate has not dropped, and
that non-operative and interventional
techniques carry their own costs and
benefits (8). Unfortunately, hepatic
ischaemia due to embolisation with
metabolic and septic complications is
a reality following such procedures.
CONCLUSION
Advances in medicine and surgery
have led up to 80% of traumatic
hepatic injuries being managed nonoperatively, with no associated rise in
mortality. In general this is applicable
to lower grades of hepatic injuries,
but with proper patient selection,
higher grades can be managed nonoperatively. However, one must
remember that conclusions from
NOPM have been deduced from
retrospective studies and as such must
be interpreted with caution. Patients
who are haemodynamically unstable
require operative intervention and the
use of damage control techniques to
achieve haemostasis, thereby allowing
full resuscitation of the patient.
Although the management of liver
trauma has evolved over the recent
decades, no guideline will ever be
a substitute for clinical judgement
and multi-disciplinary input amongst
surgeons, radiologists and emergency
physicians.

MSJA RESEARCH PAPERS

REFERENCES
1.
Pringle JH. Notes on the arrest of
hepatic haemorrhage due to trauma.
Ann Surg. 1908;48:541.
2.
Schrock T, Blaisdell FW, Mathewson C Jr. Management of blunt trauma
to the liver and hepatic veins. Arch
Surg. 1968;96:698-704.
3. Omoshoro-Jones JA, Nicol AJ, Navasaria PH, Zelweger R, Krige EJ, Kahn
DH. Selective Non-operative management of liver gunshot injuries. BJS.
2005;92:890-5.
4. David Richardson J, Franklin GA, Lukan JK, Carrillo EH, Spain DA, Miller FB
et al. Evolution in the management of
hepatic trauma: A 25 year perspective.
Ann Surg. 2000; 232: 324-30.
5.
Malhotra AK, Fabian AK, Croce
MA, Gavin TJ, Kudsk KA, Minard G et
al. Blunt hepatic injury: a paradigm
shift from operative to non-operative
management in the 1990s. Ann Surg.
2000;231:804-13.
6. Ahmed I, Beckingham, IJ. Liver trauma. Trauma. 2007;9:171-80.
7.
Nicholas JM, Rix EP, Easley KA,
Felliciano DV, Cava RA, Ingram WL
et al. Changing patterns in the management of penetrating abdominal
trauma: the more things change, the
more they stay the same. J Trauma.
2002;55:1095-110.
8.
Hurtuk M, Reed RL 2nd, Esposito
TJ, Davis KA, Luchette FA. Trauma surgeons practice what they preach: the

NTDB story on solid organ injury management. J Trauma. 2006;61:243-55.


9.
Strong RW, Lynch SV, Wall DR, Liu
CL. Anatomic resection for severe liver
trauma. Surgery. 1998;123:251-7.
10. Moore EE, Cogbill TH, Jurkovich GJ,
Shackford S, Malangoni M, and Champion H. Organ injury scaling: spleen
and liver (1994 Revision). J Trauma.
1995;38 (3):323-4.
11. Fang JF, Wong YC, Lin BC Hsu YP,
Chen MF. The CT risk factors for need of
operative treatment in initially haemodynamically stable patients after blunt
hepatic trauma. J Trauma. 2006;61:54753.
12.
Schnuriger B, Inderbitzin D,
Schafer M, Kickuth R, Exadaktylos A,
Candinas D. Concomitant injuries are
an important determinant of outcome
of high grade blunt hepatic trauma.
BJS. 2008;96:104-10.
13. Piper GL, Peitzman AB. Current
management of hepatic trauma. Surg
Clin N Am. 2010;90:775-85.
14.
Oschner MG. Factors of failure for nonoperative management of
blunt liver and splenic injuries. World J
Surg. 2001;25:1393-6.
15.
Ackroyd FW, Pollard J, Mcdermott WV. Massive hepatic resection in
the treatment of severe liver trauma.
Am J.Surg. 1968.
16.
Rotondo MF, Schwab CW, McGonigal MD, Phillips GR, Fruchterman
TM, Kauder DR et al. Damage control:
an approach for improved survival in

exsanguinating penetrating abdominal


injury. J Trauma. 1993 Sep;35(3):375-82;
17.
Avarello J, Cantor M. Pediatric
major trauma: an approach to evaluation
and management. Emerg Med Clin N Am.
2007;25:803-36.
18.
Feigin E, Aharonson-Daniel L, Savitsky B, Steinberg R, Kravarusic D, Stein M,
et al. Conservative approach to the treatment of injured liver and spleen: association with reduced mortality. Pediatric Surg
Int. 2009;25:583-6.
19.
Dicker RA, Sartorelli KH, McBride
WJ, Vane DW. Penetrating hepatic trauma
in children: operating room or not? J Pediatric Surg. 1996;31:1189-93.
20.
Meredith JW, Young JS, Bowling J,
Roboussin D. Nonoperative management
of blunt hepatic trauma: the exception or
the rule? J Trauma. 1994;36:529-35
21.
Grisoni ER, Gauder MWL, Izant RJ:
Non-operative management of liver injuries following blunt abdominal trauma in
children. J Pediatric Surg. 1984;19:515-18
22.
Mikrogianakis A. Penetrating abdominal trauma. Clin Ped Emergency Med
2010;11:217-24.
23.
Cotton BA, Nance ML. Penetrating trauma in children. Semin Pediatr Surg.
2004 May;13(2):87-97
24.
Velmahos GC, Toutouzas KG, Radin
R,Chan L, Demetriades D. Nonoperative
treatment of blunt injury to solid abdominal organs: a prospective study. Arch Surg.
2003;138:844-51

CALL FOR SUBMISSIONS


S u b m i s s i o n s a r e o p e n o n l i n e ye a r
round
Vi s i t o u r we b s i t e m s j a . e d u . a u t o
view the submission
guidelines
10

MSJA Volume 3 Issue 1 June 2011